Alice Park

Alice Park

Alice Park is a staff writer at TIME. Since 1993, she has reported on the breaking frontiers of health and medicine in articles covering issues such as AIDS, anxiety and Alzheimer's disease. Her latest book is The Stem Cell Hope: How Stem Cell Medicine Can Change Our Lives.

Is Halal Meat Healthier than Conventional Meat?

Halal refers to Muslim criteria for how food is raised slaughtered and prepared. But do the requirements make the food healthier?

Correction appended, July 30

Denmark announced last year it would ban Halal and Kosher slaughtering practices. Halal meat is reared—and slaughtered—differently from conventional meat. But is it healthier?

Like kosher food, Halal food is guided by religious criteria that govern everything from how the animals destined to be eaten are fed and raised, to how they are slaughtered and prepared for consumption.

According to the Muslims in Dietetics and Nutrition, a member group of the Academy of Nutrition and Dietetics, Halal food can never contain pork or pork products (that includes gelatin and shortenings), or any alcohol. Rasheed Ahmed, founder and president of the Muslim Consumer Group (MCG), which both certifies Halal food and educates Muslims about different foods’ Halal status, says that to be truly Halal, how the animals are raised is taken into account. Animals must be fed vegetarian diets, which means that many chickens and cows raised on U.S. farms don’t qualify (some feed contains animal byproducts). Halal animals also can’t be treated with antibiotics or growth hormones, since the hormones may contain pork-based ingredients.

Halal animals must be slaughtered by a Muslim, who says a blessing, and by hand, not by machine (which is the way many chickens in the U.S. are killed. Once killed, the animal’s blood must drain completely, since Muslims who eat Halal do not consume the fresh blood of animals.

Ahmed admits that his criteria for certification are a bit stricter than others; for example, MCG won’t certify fish if it’s farm-raised, since it’s not clear whether they fish was fed animal byproducts. Only wild-caught fish are Halal certified by MCG standards.

While some people believe that these criteria make Halal food healthier, Carol O’Neil, professor of nutrition and food sciences at Louisiana State University Agricultural Center says that there simply aren’t studies showing that to be true. The U.S. Department of Agriculture, which serves as the reference for nutritional content of food, does not separate out Halal meat (or kosher meat, for that matter) from other meats for its nutritional information.

“It’s difficult to know if there are any kind of nutritional differences,” says O’Neil. “There are certainly no studies done looking at people who consume Halal meat to see if their cholesterol levels are different, or anything like that. We just don’t know.”

O’Neil does note, however, that Halal practices may be more humane for the animal, and therefore that may make a difference for some people. “Our religion does not allow us to put any pressure on the animals,” says Ahmed. “So we treat them as humanely as possible.”

Correction: The original version of this article misstated when the ban was enacted. It was in February of 2014.

Premature Babies Are More Likely to Develop This Personality Type

Whether babies are born early can affect the personality traits they develop later, suggests the latest research

How gregarious you are, whether you tend to be anxious all the time and how responsible you are for your own actions certainly depend on a myriad of factors. Genetics, your home and school environment during childhood, as well as early life experiences, all contribute to the type of person you become.

The researchers studied a group of 200 people who were either born when they were less than 32 weeks old or with very low birth weight, both of which have been linked to other health issues in previous studies. These 200 people were compared on personality traits to 197 others born to term and of normal birth weight when all of the people in the study were 26 years old. The group of people born early or of low birth weight were more likely than the controls to fit into what the authors call a socially withdrawn personality; these people scored higher on traits of introversion, neuroticism and autistic features, while scoring lower on risk taking and agreeableness.

All told, premature birth accounted for about 11% of the personality assessment, the researchers say. That’s just a fraction of the different experiences that make up personality, but it’s possible that early birth can set children up for certain traits for a number of different reasons. Biologically, it’s possible that the premature birth exposes infants to a potentially traumatic environment in a neonatal intensive care unit that’s very different from the nurturing, calm experience of babies born to term who are immediately allowed to bond both physically and emotionally with their parents. Second, premature babies may be exposed to certain treatments, including corticosteroids, that can change their metabolic and hormonal development, priming them to be more sensitive to stress and anxiety, for example. And concerned parents of premature infants may tend to be over-protective of their children throughout childhood, contributing to the child’s tendency to avoid risk and worry more.

While personality can’t be traced to one particular experience or event, the scientists suggest that prematurity should be investigated further as a potentially important aspect of personality development. “Defining a general personality profile and understanding its aetiology are important because this higher order personality factor may help to partly explain the social difficulties [prematurely born] individuals experience in adult roles, such as in peer and partner relationships and career,” the authors write.

This New FDA-Approved Cholesterol Drug Is a Game Changer

The FDA approved the first of a new class of drugs for treating high cholesterol. Here’s the story of how researchers went from a DNA mutation to a drug in 10 years

On Friday, the U.S. Food and Drug Administration (FDA) approved the first new class of cholesterol-lowering drugs since the statins flooded the market beginning in the 1980s. Similar to the way statins work, by binding up cholesterol made in the liver so less of it circulates in the blood, this new class, called PCSK-9 inhibitors, takes advantage of genetic mutations that regulate the level of LDL receptors in the liver. Less PCSK9 leads to more LDL receptors that can soak up LDL and therefore leave less cholesterol in the blood.

The FDA approved alirocumab (Praluent), an injectable drug made by Sanofi and Regeneron, in people with familial hypercholesterolemia, a genetic condition in which cholesterol levels are high, or those with a history of heart disease who can’t reduce their LDL levels enough with existing statin drugs. (Another PCSK9 inhibitor, evolocumab (Repatha) developed by Amgen, received approval in Europe but won’t be evaluated by the U.S. FDA until the end of August.)

While PCSK9 drugs help to lower cholesterol, the story of how these medications developed began in a French family with the opposite problem. Their members had exceptionally high levels of LDL and greater than average rates of heart disease. But unlike others with similar cholesterol problems, this family did not have the usual mutations in cholesterol-regulating genes. Instead, French researchers studying them in 2003 found they had aberrations in PCSK9, a gene that produces a protein found primarily in the liver, kidneys and intestines.

An ocean and half a continent away, Jonathan Cohen and Dr. Helen Hobbs at the University of Texas, Southwestern Medical Center in Dallas (coincidentally the same institute where scientists discovered LDL, or the heart-disease contributing cholesterol and earned the Nobel Prize for their work), read the description of PSCK9 and wondered whether those with lower levels of PCSK9 would show the opposite effect of the French family and actually enjoy decreases in levels of LDL in the blood.

Cohen and Hobbs were involved in a large heart disease study involving nearly 15,000 participants, and decided to look for the PCSK9 mutations among their participants. They homed in on those with the highest and lowest levels of LDL cholesterol, and sequenced their genomes to see if any patterns emerged. Sure enough, they found 33 people whose LDL levels were about 40% lower than average and who shared mutations that effectively silenced PCSK9. Essentially, their LDL amounts were about the same as those who relied on statins to drop their cholesterol.

These PCSK9 mutations associated with the lowest LDL appeared predominantly in African-American participants. Those with one copy of the mutation in this gene showed an 88% lower risk of heart disease. Another mutation in the same PCSK9 gene that appeared more commonly in whites had the same effect, but to a lesser extent, dropping LDL by 15% and the risk of heart events by 47%.

To confirm this, Cohen searched for anyone in the study with two copies of the mutation, to see if having double the effect would trigger any adverse events. He found one woman, a 32 year old daughter of one of the participants, who had two different mutations in each of the PCSK9 copies she inherited from her mother and father. The result? An LDL of 14 and no other health problems. “If you measure the amount of PCSK9 in her blood, it’s basically absent, you can’t see any,” says Cohen. That contributed to an unprecedented low level of LDL cholesterol as well.

So far, he says, only one other individual has been described with two mutant copies of PCSK9, a 21 year old woman living in south Africa with an LDL of 20.

Those descriptions piqued the interest of researchers at Regeneron, a biotech company that specializes in turning genetic discoveries like this one into drugs. To confirm and better understand the effects of PCSK9, researchers there studied the effect of human versions of PCSK9 in mice, and then began trials of antibodies they developed that inhibit the function of this gene, much like the mutations do, in several thousand people.

Those results, published in the NEJM last April, showed that PCSK9 inhibitors can lower LDL cholesterol by an additional 60% on average beyond that achieved by statins. Those findings formed the basis of the companies’ application to the FDA for approval of these first-in-class drugs.

For now, the agency says the drugs should only be prescribed to people with familial hypercholesterolemia, or those who have failed to reduce their LDL levels sufficiently using statins. For many, the new drugs will be taken in combination with statins and a heart-healthy diet. But doctors say they anticipate many patients outside of these groups, who have family histories of heart disease or other risk factors, such as hypertension or diabetes, may start asking about the medications. For them, doctors will have to weigh how well they are doing on statins before considering adding a PCSK9 inhibitor.

At the annual Alzheimer’s Association International Conference in July 2015, scientists report some encouraging news about the benefits of exercise. In the first studies to look at physical activity among people already diagnosed with the early stages of Alzheimer’s, moderate to high intensity workouts may not only slow down the biological symptoms of Alzheimer’s—but may lead to improvements in cognitive functions as well.

In one study involving 200 people with mild or moderate disease, Dr. Steen Hasselbalch from the University of Copenhagen and his colleagues randomly assigned some participants to an hour of exercise three times a week for 16 weeks, while allowing the remainder to continue without a regular activity regimen. After a phase-in period, the exercisers were working at a moderate to intense level, achieving 70% to 80% of their maximum heart rate for at least half of each session.

That level of intensity is important, says Hasselbalch, to achieve results. Compared to the control group, the exercisers showed fewer symptoms such as anxiety, changes in mood and depression that are common among Alzheimer’s patients. Overall, those who were more active did not show any changes in cognitive functions, but when Hasselbalch looked at the results more carefully, he found that participants with milder disease who exercised actually did perform better on intellectual skills after the 16 weeks. They were tested on memory, language, mental speed and other executive functions.

“It’s been shown with other diseases that exercise can have beneficial effects,” he says. “Now we have shown it’s also important for dementia. So if you now have this alternative treatment, it sends a message that you can do something even after diagnosis to treat dementia.”

Because the people exercised in a group setting, he says that simply being part of that social situation and getting out of the house and interacting with others appears to reduce the mood-related symptoms of Alzheimer’s. “But if you really want an effect on cognition, then you have to exercise hard.”

He admits that his study did not delve into how the exercise might be contributing to the improved cognitive changes, but he will be analyzing the blood and cerebral spinal fluid collected from the participants to study that further.

Such changes are what Laura Baker, from Wake Forest School of Medicine, and her team did with another group of early stage Alzheimer’s patients. They wanted to see what biological changes exercise might have on the Alzheimer’s process, and focused on 70 patients with mild cognitive impairment and diabetes, both of which significantly increase the risk for Alzheimer’s. Some were randomly assigned to simple stretching exercises, while others were told to exercise four times a week and, like those in Hasselbalch’s study, had to work hard enough to raise their heart rate to 70% to 80% of its maximum for 30 of the 45 minutes of each session. Baker then studied their cognitive function tests, brain imaging and levels of Alzheimer’s proteins in their cerebral spinal fluid.

She found that those who exercise rigorously increased the blood flow in the areas of the brain responsible for memory and higher level processing. The result was a dramatically increased score, by 80%, on average on the cognitive tests than those who just stretched, even after accounting for age-related changes in thinking. More intriguing, the exercisers also showed on average a 14% lower level of the protein tau, which is a good indicator that brain neurons are dying and Alzheimer’s processes are well underway, at the end of the study compared to before they began the exercise regimen.

“What’s encouraging to us is that we don’t have treatments now; there’s nothing for Alzheimer’s patients,” says Baker. “The possibility that a non-medicine intervention could actually change the disease — we’re just very encouraged by these results,.”

While the exercise regimen wasn’t an easy one — it qualifies as moderately intense physical activity, which for a group of older adults who are likely sedentary to begin with is certainly a challenge, both Hasselbalch and Baker say that with the right execution — by working with participants and by gradually increasing their exercise level — achieving the amounts of activity needed to help their brains is possible. Baker also points out that it’s time to start studying the combined effects of new medications that are being tested for Alzheimer’s and increased physical activity. Together, she says, they may hold the key to actually slowing down and possibly even reversing progression of the disease.

When Chemotherapy Does More Harm than Good

Chemotherapy has saved countless lives and is a mainstay of cancer care. But the latest data suggests that it can also do more harm than good for some patients

A cancer diagnosis is a life-altering event, and the news—let alone making decisions about how to manage treatment—is already challenging enough. But with a terminal diagnosis, those choices become even more fraught. At some point, say ethicists, doctors and patient advocates, enough is enough. Meaning the potential for benefit has to be weighed against the quality of what life is likely to be left. But where is that line? And how does each patient find it?

A study published inJAMA Oncology highlights just how agonizing those choices can get. Holly Prigerson, director of the Center for Research on End of Life Care at Weill Cornell Medical College and her colleagues studied the use of chemotherapy among a group of 312 terminal cancer patients. All had been given no more than six months by their doctors, and had failed at least one if not multiple rounds of chemotherapy, seeing their tumors spread to other parts of their body. About half were on chemotherapy, regardless of its ineffectiveness, at the time of the study.

Despite the intuitive sense that any treatment is better than none, there is not much evidence that chemotherapy is the right choice in these cases—and it may very well be the wrong one. Prigerson’s analysis showed that these patients experience a drop in their quality of life if they get chemo, and that they are therefore worse off than if they hadn’t opted for the treatment. On measures of things like whether they could continue to walk on their own and take care of themselves and keep up with their daily activities, those on chemotherapy reported marked declines compared to patients who opted not to receive more chemo.

“The results were counterintuitive to some extent,” says Prigerson. “The finding that the quality of life was impaired with receipt of the toxic chemotherapy was not surprising. The surprising part was that people who were feeling the best at the start of the therapy ended up feeling the worst. They are the ones most harmed and who had the most to lose.”

In other words, the chemo made the patients feel worse without providing any significant benefit for their cancer.

Previous studies have showed that chemotherapy in terminal patients is essentially ineffective; among those with non-small cell lung cancer, for example, third rounds of chemo were associated with a 2% response rate in tumor shrinkage, while fourth rounds showed 0% response. And whatever tumor shrinkage occurred wasn’t linked to a longer life.

Groups like the American Society of Clinical Oncologists (ASCO) recently advised doctors to be more judicious with their chemotherapy use in terminal patients. The group’s guidelines recommend limiting it to relatively healthy patients who can withstand the toxic treatment and potentially overcome side effects.

The decision about how long to continue care, including chemotherapy, is up to each cancer patient, but Prigerson hopes that her results help to better inform those choices in coming years. Recent studies showed, for example, that despite explanations from their doctors, many cancer patients still believe that more rounds of chemo will provide some benefit to them, and are therefore—and understandably—reluctant to stop receiving therapy. But at some point, the data shows, more treatment is not better.

That may be especially true of patients with end-stage cancer who are still relatively healthy and not feeling sick. For them, additional chemotherapy will likely make them weaker, not to mention eat up more of the precious time they have left traveling to and from infusion centers. Prigerson plans to continue the study to better understand the dynamics of how decisions about treatments are made toward the end of life, but in the meantime hopes the latest findings at least convince doctors to reconsider how they advise their terminal patients about end-stage chemotherapy.

Noteworthy Advances in Alzheimer’s Research

At the latest gathering of the world’s experts on Alzheimer’s disease in late July there was encouraging news–and sober reminders of how challenging the degenerative brain disease can be. The need for better ways to both screen for and treat the condition is urgent: 1 in 3 seniors dies of some kind of dementia. …

Scientists have been warning for decades that we use too many antibiotics, both in people to treat relatively mild infections and in agriculture to bulk up farm animals and keep them free of disease. The consequences, they caution, are dire—and already emerging in hospitals with bacteria that can’t be treated with any of our existing antibiotic medications.

But the thinking went that to become resistant to the drugs we use on them, bacteria have to pay a price. They may be able to survive the pharmaceutical onslaught, but they’re less fit and therefore less able to reproduce, less likely to remain for long in their host of choice and otherwise sapped of the energy needed to really wreak havoc on human or animal immune systems.

At least, that was the theory (and perhaps the hope) until now. In a study published in Science Translational Medicine, however, researchers show how misguided that belief is. Delving into the genetic code of certain common bacteria such as Pseudomonas aeruginosa and Acinetobacter baumannii — both of which are resistant to multiple antibiotics— and Vibrio cholerae, the researchers identified genes that change in the presence of these drugs. In animal models, they observed how these changes affected the different bacteria’s ability to infect and populate in hosts.

To their surprise, rather than being compromised, the antibiotic-resistant bacterial strains seemed to be stronger, more robust and better able to infect cells than less resistant strains.

“With all the possible mutations in the bacteria, there is a battle royale, a competition among all the mutants, and we see that the most fit, the most virulent were the ones that were resistant to the antibiotics,” says Dr. David Skurnik, senior author of the paper and assistant professor of medicine at Brigham and Women’s Hospital and Harvard Medical School. In the case of P. aeruginosa, he says, “the acquisition of antibiotic resistance was associated with the most increased fitness in all the possible mutations in P. aeruginosa.”

That means that the problem of antibiotic-resistant bugs just got more complicated. Overuse of antibiotics increases the number of bacterial strains that have mutations which make them better able to withstand the drugs, and this latest research shows that these strains may also be more adept at infecting hosts and causing disease. “We’ve gotten a double whammy with the acquisition of antibiotic resistance,” says Gerald Pier, a co-author of the paper and professor of medicine, microbiology and immunobiology at Brigham and Harvard Medical School. “Not only does antibiotic resistance make it more difficult to treat infections because we have fewer drugs they will respond to, but it makes the organism better able to cause infection.”

While still important, the conventional solution of cutting back on antibiotic use may not be enough, he says. Using antibiotics more appropriately will certainly reduce the appearance of new drug-resistant strains, but it won’t be enough to tamp down the emergence of these fitter, more virulent bacteria that also happen to be adept at evading the effects of antibiotics. For that, he says, other infection-fighting strategies, including boosting the immune system with vaccines or antibody treatments, may be needed.

That’s what Pier and Skurnik are working on currently, and so far, they’ve developed encouraging options for treating infections that may keep the more robust bacteria at bay. They’re targeting parts of bacteria that many strains have in common and developing new says to recognize these targets and neutralize the bacteria so they can’t cause serious infections and disease. “These results show that, yes, the problem of multi-drug resistant bacteria is more complex than we thought, but there are solutions,” says Skurnik.

Two New Alzheimer’s Drugs Offer Hope—With Caveats

Reports on two compounds provide limited optimism in the search for pharmaceutical answers to treating Alzheimer’s disease

Reporting at the Alzheimer’s Association International Conference in Washington, D.C., researchers showed some glimmers of hope in the potential benefit of two agents being tested in patients with mild to moderate Alzheimer’s disease. Currently, there are no treatments that address the root causes of the neurodegenerative condition, which include the build up of amyloid plaques in the brain and the formation of tau tangles once nerve cells start to die off.

One drug, from Eli Lilly, aims to soak up amyloid and thus prevent it from accumulating in the damaging plaques that suffocate neurons in the brain. But to test its effectiveness in a timely manner, the scientists adopted an unorthodox trial design — they divided participants with mild to moderate disease into two groups, one that took the drug, which is given via IV, and another that took placebo. After 18 months, there were no significant differences between the groups on cognitive tests, although people with mild disease seemed to show signs of improvement. So those on placebo were then switched to the study drug, called solanezumab, and followed for another 18 months to two years. The idea was that by the end of the study, the participants who had been taking the drug all along should show greater improvements in cognitive skills than those who switched midway through.

That’s what the researchers saw. In their report, they said that the two groups showed differences in their thinking abilities. But whether that gap can be attributed to the drug alone isn’t entirely clear—at least not yet. And whether that difference is enough to fuel further study, especially in people at the earliest stages of the disease, or form the basis of an approval by the Food and Drug Administration is even more uncertain.

The other experimental agent, aducanumab, also sops up amyloid, but was associated with brain swelling in earlier studies at higher doses. Scientists at Biogen, which is developing the compound, added an intermediate dose to get a better sense of how much of the drug could produce the most benefit without triggering side effects. The results were from an earlier stage of testing, and focused primarily on safety of these doses so developers could not say for certain whether the improvements they began to see in slowing cognitive decline were significant. But they were enough to warrant more study.

Both trials show that, while promising, the first-ever treatments for Alzheimer’s have a ways to go still on this long, and often precarious road.

Why We Still Need Fetal-Tissue Research

Two sting videos that claim to implicate Planned Parenthood in the illegal practice to selling fetal tissue for a profit prompted a Congressional investigation of the organization. But it doesn’t mean that research on fetal tissue is wrong. Or that it should be stopped.

Fetal tissue is valuable for medical research; the National Institutes of Health spent $76 million on fetal research in 2014, and fetal tissue has contributed to vaccines for polio, rubella and chicken pox. While recent efforts to transplant fetal tissue to treat conditions like Parkinson’s haven’t been as consistently successful, it’s still critical to scientific progress.

In the video, Dr. Deborah Nucatola, senior director of medical services, notes that the fees Planned Parenthood charges are within laws that govern fetal tissue procurement; the fees cover the expenses of handling, storing and shipping the material, not for the material itself. But in calling for the Congressional investigation into Planned Parenthood’s practices, House Speaker John Boehner said: “When an organization monetizes an unborn child — and with the cavalier attitude portrayed in this horrific video — we must all act.”

But there’s a blurring of the ethical and political lines here that is both intentional — and intentionally misleading. It’s one that’s always shadowed anything involving fetal tissue in this country. Fetal tissue research was initially allowed under specific conditions and approval by a government Ethics Advisory Board (EAB). During the 1980s, however, as controversy over the source of the fetal tissue — mostly abortions, and primarily elective ones — became increasingly politicized, a moratorium was placed on fetal tissue studies, and the EAB was disbanded. The restriction was lifted in 1993, but the work continued to be a challenge.

The ethical and political conflicts erupted again in 1998, when researchers studying excess IVF embryos and fetuses from elective abortions made breakthroughs in understanding stem cells, the pre-cells of everything that develops in the human body. The promise represented by these stem cells, which because of their developmental potential can possibly be manipulated to replace diseased or ailing cells, raised anew the questions of whether studying tissues from unused embryos and aborted fetuses was ethically — and politically — acceptable.

The resulting debate hampered stem cell research in the U.S. for nearly a decade, after the George W. Bush Administration prevented federal research money from being used to study excess embryos that couples had donated after IVF. Researchers wanting to pursue this work had to find private funding or leave the country, which some did. President Obama lifted the restriction in 2009 — and now, the controversy has erupted again. And as in times past, science is getting muddied by politics.

“This video is primarily aimed not at fetal tissue research but at Planned Parenthood,” says David Magnus, director of the Stanford University Center for Biomedical Ethics. “I don’t think this is about the use of tissue that is already discarded. I think it’s about abortion itself. The fact that it’s not clear whether there is any actual problem in terms of [Planned Parenthood’s] behavior highlights the fact that this is politically motivated.” Several Republican presidential candidates have also criticized Planned Parenthood’s practices, invoking the organization’s “disregard for the culture of life” and it’s “penchant for profiting off the tragedy of a destroyed human life.”

There’s no evidence on the video that Planned Parenthood makes a profit from fetal tissue. Nucatola is recorded as saying the organization pays anywhere from $30 to $100 per specimen, and that those fees cover administrative and handling costs, not the cost of the tissue itself. (Those costs are far lower than what other companies that broker exchange of tissues from hospitals and abortion clinics to those who want to study them charge.)

Women who decide to have abortions are asked after they make their decision about whether they want to donate the fetus to research. But not every woman is even given the choice. Similar to marijuana laws, in which there is a disconnect between federal and state policies governing its legality, federal law allows donation of fetal tissue if there is no payment involved, and it doesn’t influence the woman’s decision to have an abortion, while state policies may differ.

“State and local policies, as best I can tell, are patchwork, and there is no consistency across states with regard to how [fetal] tissues are used, whether or not they are allowed to be used, etcetera,” says Debra Mathews, assistant director for science programs at the Berman Institute of Bioethics at Johns Hopkins University. According to the Guttmacher Institute, six states currently prohibit fetal tissue research on aborted fetuses; three states have introduced similar statues that were struck down. And adding to the confusion, some states prohibit experimentation on “live” fetuses, attempting to make distinctions between the state of the fetus following the procedure.

Such opaque policies, and the highly contentious nature of discussing anything involving fetuses, makes it nearly impossible to fully inform women and discuss their choices in an objective way. With embryonic stem cell research, which involves use of embryos that couples donate for research, Mathews notes that there were discussions about the ethical and moral questions involved. “I don’t know that we have had robust conversations about fetal tissue,” she says. “It’s very difficult to talk about. Abortion politics in this country make it very difficult to have discussions about the use of these tissues.”

And that’s led to a situation that’s far from open when it comes to the fate of fetal tissue from abortions. “There is important research, good research, involving fetal tissues,” says Mathews. “But we have not been transparent about it. In so far as this increases the transparency, and helps us to have a conversation about the research being done, and folks are following the rules that do exist, I think that’s important.”

That may be nearly impossible, however, if conservative politicians continue to corral abortion positions and fetal research positions into the same ethical pen. Magnus notes that those opposed to abortion can still support fetal tissue research, and that the two stances aren’t as mutually exclusive from an ethical perspective. “The analogy is often made of organ procurement. ‘I’m not in favor of car accidents or people shooting each other. But if tragedies happen, and somebody is shot or there is a car accident, then being able to have something good come out of that is seen largely as a good thing.’”

One question the Congressional investigation will consider is whether the decision to donate the tissue influences the way in which abortions are performed at Planned Parenthood — if it does, that too is unlawful. But it would only be unethical if it compromises the health of the woman in any way. In the video, Nucatola discusses the fact that the way the abortion is performed should be the same for every woman, regardless of whether she agreed to donate the fetal tissue or not. But she does admit that “some people will actually try to change the presentation [of the fetus]” and that “you’re just kind of cognizant of where you put your graspers, …we’ve been very good at getting heart, lung, liver, because we know that, so I’m not gonna crush that part…and I’m gonna see if I can get it all intact.”

Planned Parenthood’s president Cecile Richards issued an apology for the tone of the discussion, acknowledging that “This is unacceptable, and I personally apologize for the staff member’s tone and statements.”

But Richards defends the way that Planned Parenthood performs abortions as ethical and legal. “Our donation programs, like any other high-quality health care providers, follows all laws and ethical guidelines. [Women and families’] commitment to life-saving research, developing treatments for diseases like Parkinson’s and Alzheimer’s is important and compassionate. And it should be respected, not attacked,” she said in a video responding to the allegations.

But as long as the dialogue about the science and the medical potential of fetal research is entwined in the political debate over abortion, that respect — and the lives that can potentially be saved from these studies — will be hard to come by.

Dad Bod Is Explained By Science In a New Study

A first-of-its kind study to follow men for up to 20 years from adolescence shows that dads do get a little squishier after the kids

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According to Clemson student Mackenzie Pearson, who wrote a viral essay essay on the appeal of the dad bod, it’s a physique that’s a “nice balance between a beer gut and working out,” the result of going to gym but indulging in a few pizzas once in a while and being okay with that. (Think John Hamm, and Chris Pratt before he went Jurassic.)

And according to scientists, Pearson and her demographic have pretty much nailed it. The source of that “more human, natural and attractive” body is unique to fathers and can be traced to simply having kids.

In a study published in the American Journal of Men’s Health, Dr. Craig Garfield, a pediatrician at Northwestern University Feinberg School of Medicine and his colleagues dove into a database of 10,263 men beginning when they were 12 years old and followed them for up to 20 years. They looked specifically at how body mass index (BMI), a combination of height and weight, changed over time as the men either became fathers or did not, and for those who did, whether they were what the researchers called resident fathers who lived with their children, or non-residents who lived separately.

Whether or not they lived with their kids, becoming a father was linked to around a four pound increase in weight over the study period, while remaining child-free was associated with a 1.4 pound weight loss for a six-foot-tall man.

“It’s a unique look at the influence that a social phenomenon, becoming a father, has on a biological marker, namely BMI,” says Garfield. “It really plants fatherhood as a potential social determinant of health for men.”

That’s a critical finding, especially since men, and in particular young men, are typically less proactive about taking care of their health. Garfield notes that while many men will quit smoking and drink less and otherwise try to become healthier when they become fathers, there may be other factors associated with caring for kids that counteract those good intentions, such as being surrounded by more kid-friendly, high calorie foods and snacks, as well as their leftovers.

“From my own point of view, we wouldn’t have as many pizzas in the house if the kids weren’t around, and we wouldn’t have the brownies my wife makes if the kids weren’t around,” says Garfield. “Having kids around changes not only the food in the house and what is available to you for meal, but also for snacks. It also changes whether you are able to find time to get out and exercise and get enough sleep and take care of yourself.”

Dads, of course, are not alone in experiencing these effects of parenthood. But this is the first study to tease out specifically the effects of fatherhood on weight gain over time. Since men are less likely to be seeing doctors regularly, if they are joining their partners during prenatal visits or pediatric visits, says Garfield, those are good opportunities to talk to them about their own eating, exercise and sleep habits to make them aware of the sneaky way that pounds can creep up on dads and potentially affect their health (even if the look seems to have its own kind of physical appeal).